Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

In general LV remodeling represents an adaptive mechanism including LV enlargement, hypertrophy and distortion of regional and global geometry. This process involves all cells that are present in the myocardium - the myocyte, the interstitial cells, the vascular endothelium, and the immune cells (2). Despite the varying etiopathology LV remodeling is associated with a similar sequence of molecular, biochemical and mechanical events that can lead to heart failure, myocyte hypertrophy, extensive extracellular matrix production and fibrosis.

LV remodeling following myocardial infarction has been well studied in a number of studies (5,6,7,8). The acute, subacute and chronic phases of this process are described (5). The results of the studies on LV global geometry in patients with myocardial infarction demonstrated that late ventricular enlargement after anterior myocardial infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion (6). Kleber et al. (7) reported that the sphericity index is the only technical parameter able to predict LV volume increases in patients with myocardial infarction and concluded that deformation of ventricular geometry and filling pressures are major factors promoting remodeling following myocardial infarction.

DC is a heterogeneous myocardial disease. However, all dilated cardiomyopathies eventually converge toward an aspecific type of ventricular remodeling. When studying LV remodeling in patients with DC we usually deal with the late maladaptive phase of this process because of insidious clinical course of the disease.

In this study, we have demonstrated that in patients with DC significant ventricular enlargement and distortion is not accompanied by a proportional increase in wall thickness so that the thickness-to-radius ratio is not maintained. These abnormalities contribute to a marked elevation in myocardial wall stress. From the physiologic point of view the myocytes in the remodeled ventricle can no longer effectively translate their active state into shortening because of an excessive systolic wall stress. The present study has also shown that the ratio of circumferential to meridional wall stress is abnormally low in patients with DC.

LV dilation and geometric distortion are known as the main markers of LV remodeling. In this study, LV diastolic sphericity index was chosen an indicator of the progression of ventricular remodeling. Our previous studies have demonstrated that this parameter is a sensitive index of LV remodeling in patients with DC (9).

This study showed that the patients in tertiles with advanced and moderate LV remodeling had worse NYHA functional class compared to the patients in the tertile with minimal LV remodeling. Patients in the tertile with the most spherical ventricles had also the lowest exercise capacity as assessed by six-minute walk distance. As expected, a greater shape distortion was associated with increased LV volumes and decreased ejection fraction.

Similar results have been obtained by several investigators in patients with LV dysfunction of ischemic etiology. Lamas et al. (10) demonstrated the importance of LV shape in determining exercise capacity in patients with LV dysfunction after myocardial infarction. A greater geometric distortion was associated with increased LV volumes, decreased ejection fraction and a larger abnormally contracting myocardial segment. The patients in the tertile with the most spherical ventricles had not only the lowest exercise capacity, but also accumulated the highest heart failure and specific activity scale scores. Tischler et al. (11) reported that measurements of LV volumes and ejection fraction at rest did not predict exercise capacity in patients with LV dysfunction. However, dynamic changes in sphericity index correlated strongly with exercise duration and were important determinants of exercise capacity in patients with systolic LV dysfunction.

Another finding in this study is that LV diastolic sphericity index is a determinant of LV diastolic filling. We have previously observed that this index significantly correlates to Doppler-derived indices of LV diastolic filling in patients with DC (9). This study has demonstrated that the restrictive pattern of LV filling is more common in patients with moderate and advanced LV remodeling according to tertiles of diastolic sphericity index.

This study has also confirmed that LV sphericity is a factor in the etiology of mitral regurgitation in patients with DC. A greater LV shape distortion was associated with more prominent mitral regurgitation. Patients in the tertile with the most spherical ventricles had the highest degree of mitral regurgitation. These findings are consistent with data from previous studies that demonstrated that LV shape is a determinant of functional mitral regurgitation in patients with acute myocardial infarction (12) and in patients with severe heart failure (13). Our observation also lends support to previous experimental findings on the role of transformation of LV shape in the genesis of functional mitral regurgitation (14,15).

Limitations of the study. Coronary arteriography was not performed in this study. Therefore the patients group is likely to include those with idiopathic DC as well as ischemic cardiomyopathy. Medical treatment was not characterized in this study. However, the majority of patients in this study were taking the same pharmacological agents, including angiotensin-converting enzyme inhibitors and diuretics.

Conclusions. This study has shown that maladaptive ventricular remodeling in dilated cardiomyopathy is accompanied by significant left ventricular dilation and shape distortion, eccentric hypertrophy and raised end-systolic wall stress. The data indicate that the progression of ventricular remodeling in dilated cardiomyopathy is associated with more severe heart failure and deteriorated left ventricular systolic function. The prevalence of restrictive diastolic filling, as well as the degree of mitral regurgitation also depends on ventricular remodeling. These observations lend support to the concept that left ventricular remodeling is a determinant of both clinical status and cardiac function in dilated cardiomyopathy.

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